Misrepair using radiosensitizer and radiosensitivity under non cycling cells

使用放射增敏剂的误修复和非循环细胞下的放射敏感性

• 批准号: 23591849
• 负责人: KAWATA Tetsuya
• 金额: $ 3.16万
• 依托单位: Keio University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23591849/
• 关键词: 幹細胞; 静止期細胞; 放射線増感; ＰＬＤＲ; 誤修復; 癌幹細胞; 重粒子; PLDR; 腫瘍幹細胞; ATM; NBS1

We have demonstrated whether AKT is important molecular targets to control the radioresistance through the activation of phospholitated AKT compared between CD133+ and CD133- glioma tumour cells after ionizing radiation treatment. We showed IR-induced AKT phosphorylation in CD133+ tumour cells than CD133- tumour cells when mirin was used. Our data suggested that the tumour cells expressing CD133+, a maker for the stem cell, was induced the activation of AKT more than CD133- cells after radiation. From this result, it may be said that CD133+cells have greater repair activation in response to DNA damage in cellular radiosensitivity. Confluent normal cells were exposed to X-rays and heavy ions and PLDR was studied using FISH technique. It was found that heavy ions induce similar exchanges between PLDR and PLD condition, suggesting that heavy ion therapy is as effective to non-cycling cells as cycling cells.

我们通过比较电离辐射治疗后CD133+和CD133-胶质瘤细胞中磷酸化AKT的激活，论证了AKT是否是控制放射抗性的重要分子靶点。我们发现当使用mirin时，IR诱导CD133+肿瘤细胞的AKT磷酸化高于CD133-肿瘤细胞。我们的数据表明，辐射后表达干细胞标志物CD133+的肿瘤细胞比CD133-细胞更能诱导AKT的激活。从这一结果可以说，CD133+细胞在细胞辐射敏感性方面对DNA损伤具有更大的修复活性。融合的正常细胞暴露于X射线和重离子，并用FISH技术研究PLDR。结果发现，重离子引起PLDR和PLD状态之间的交换相似，表明重离子治疗对非周期细胞和周期细胞同样有效。